scholarly journals Impact of chromosome 17q deletion in the primary lesion of colorectal cancer on liver metastasis

2016 ◽  
Vol 12 (6) ◽  
pp. 4773-4778 ◽  
Author(s):  
Masaya Kawai ◽  
Hiromitsu Komiyama ◽  
Masaki Hosoya ◽  
Haruna Okubo ◽  
Tomoaki Fujii ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Primary Lesion ◽  
Chromosome 17Q

PET-CT Standard uptake value predict bevacizumab-containing chemotherapy response and prognosis for unresectable colorectal cancer liver metastasis

2019 ◽  
Author(s):  
Yang Lv ◽  
QingYang Feng ◽  
WenTao Tang ◽  
YuQiu Xu ◽  
SongBin Lin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Tumor Size ◽  
Metastatic Tumor ◽  
Standard Uptake Value ◽  
Primary Lesion ◽  
First Line ◽  
Colorectal Cancer Liver Metastasis ◽  
Pet Ct ◽  
Line Chemotherapy

Abstract Background: Standard uptake value (SUV) of PET-CT is an indicator of tumor metabolic response. In this paper, we aim to explore the clinical value of SUV on the unresectable colorectal cancer liver metastasis (CRLM) patients receiving bevacizumab-containing chemotherapy. Method: This study was performed retrospectively. A total of 185 CRLM patients between April 2011 to December 2015 with complete clinical data were included in this study. All the enrolled patients were assigned into two treatment cohorts (bevacizumab plus first-line chemotherapy cohort and chemotherapy only cohort). A blindly, independent radiologist evaluated images for RECIST and morphologic response. All clinical variables, and various PET/CT parameters were statistically compared with progression-free survival (PFS) and overall survival (OS). Primary and Metastatic tumor SUV were selected for analysis. Results: Among the 185 patients, 101 patients received first line chemotherapy plus bevacizumab (beva cohort), 84 patients only received first-line chemotherapy (CMT cohort). Baseline characteristics of two cohorts showed no statistical difference (P>0.05). Primary SUV level was correlated with primary tumor size, while metastatic SUV was statistically correlated with metastatic tumor number and tumor size (P=0.000). Primary lesion, metastatic lesion SUV and elevation of SUV demonstrated prognostic role for OS (P<0.05). SUV gap were statistically associated with optimal response in bevacizumab cohort (P=0.03) and no-PD status in chemotherapy cohort (P=0.019), respectively. After multivariate analysis, elevated SUV is an independent risk factor for OS (P=0.000). Besides, elevation of SUV between metastatic and primary lesion can be a predictive factor for bevacizumab survival benefit. Conclusion: PET-CT scan is important for CRLM patients. Our study demonstrated that an elevation of SUV was a better prognostic and predictive marker for CRLM patients.

scholarly journals The prognostic role of KRAS and BRAF in patients undergoing surgical resection of colorectal cancer liver metastasis: a systematic review and meta-analysis

2016 ◽  
Vol 27 ◽  
pp. iv41
Author(s):  
F. Passiglia ◽  
A. Galvano ◽  
S. Rizzo ◽  
A. Listì ◽  
N. Barraco ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Systematic Review ◽  
Liver Metastasis ◽  
Surgical Resection ◽  
Meta Analysis ◽  
Prognostic Role ◽  
Colorectal Cancer Liver Metastasis

Stem cell gene Girdin: a potential early liver metastasis predictor of colorectal cancer

2012 ◽  
Vol 39 (9) ◽  
pp. 8717-8722 ◽  
Author(s):  
Chen Liu ◽  
Hongpeng Xue ◽  
Yixia Lu ◽  
Baorong Chi
Keyword(s):  
Colorectal Cancer ◽  
Stem Cell ◽  
Liver Metastasis ◽  
Cell Gene ◽  
Stem Cell Gene

scholarly journals Liver Immune Microenvironment and Metastasis from Colorectal Cancer-Pathogenesis and Therapeutic Perspectives

Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2418
Author(s):  
Xuezhen Zeng ◽  
Simon E. Ward ◽  
Jingying Zhou ◽  
Alfred S. L. Cheng
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Cancer Patients ◽  
High Recurrence Rate ◽  
Immune Microenvironment ◽  
Liver Sinusoidal Endothelial Cells ◽  
Premetastatic Niche ◽  
Cancer Pathogenesis ◽  
Colorectal Cancer Patients ◽  
The Impact

A drastic difference exists between the 5-year survival rates of colorectal cancer patients with localized cancer and distal organ metastasis. The liver is the most favorable organ for cancer metastases from the colorectum. Beyond the liver-colon anatomic relationship, emerging evidence highlights the impact of liver immune microenvironment on colorectal liver metastasis. Prior to cancer cell dissemination, hepatocytes secrete multiple factors to recruit or activate immune cells and stromal cells in the liver to form a favorable premetastatic niche. The liver-resident cells including Kupffer cells, hepatic stellate cells, and liver-sinusoidal endothelial cells are co-opted by the recruited cells, such as myeloid-derived suppressor cells and tumor-associated macrophages, to establish an immunosuppressive liver microenvironment suitable for tumor cell colonization and outgrowth. Current treatments including radical surgery, systemic therapy, and localized therapy have only achieved good clinical outcomes in a minority of colorectal cancer patients with liver metastasis, which is further hampered by high recurrence rate. Better understanding of the mechanisms governing the metastasis-prone liver immune microenvironment should open new immuno-oncology avenues for liver metastasis intervention.

scholarly journals LncRNA MIR17HG promotes colorectal cancer liver metastasis by mediating a glycolysis-associated positive feedback circuit

Oncogene ◽  
2021 ◽  
Author(s):  
Senlin Zhao ◽  
Bingjie Guan ◽  
Yushuai Mi ◽  
Debing Shi ◽  
Ping Wei ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Metastatic Tumor ◽  
Feedback Circuit ◽  
Colorectal Cancer Liver Metastasis ◽  
Positive Feedback Circuit

AbstractGlycolysis plays a crucial role in reprogramming the metastatic tumor microenvironment. A series of lncRNAs have been identified to function as oncogenic molecules by regulating glycolysis. However, the roles of glycolysis-related lncRNAs in regulating colorectal cancer liver metastasis (CRLM) remain poorly understood. In the present study, the expression of the glycolysis-related lncRNA MIR17HG gradually increased from adjacent normal to CRC to the paired liver metastatic tissues, and high MIR17HG expression predicted poor survival, especially in patients with liver metastasis. Functionally, MIR17HG promoted glycolysis in CRC cells and enhanced their invasion and liver metastasis in vitro and in vivo. Mechanistically, MIR17HG functioned as a ceRNA to regulate HK1 expression by sponging miR-138-5p, resulting in glycolysis in CRC cells and leading to their invasion and liver metastasis. More interestingly, lactate accumulated via glycolysis activated the p38/Elk-1 signaling pathway to promote the transcriptional expression of MIR17HG in CRC cells, forming a positive feedback loop, which eventually resulted in persistent glycolysis and the invasion and liver metastasis of CRC cells. In conclusion, the present study indicates that the lactate-responsive lncRNA MIR17HG, acting as a ceRNA, promotes CRLM through a glycolysis-mediated positive feedback circuit and might be a novel biomarker and therapeutic target for CRLM.

scholarly journals Targeting BMI-1-mediated epithelial–mesenchymal transition to inhibit colorectal cancer liver metastasis

2020 ◽  
Author(s):  
Zhiyao Xu ◽  
Zhuha Zhou ◽  
Jing Zhang ◽  
Feichao Xuan ◽  
Mengjing Fan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Colorectal Cancer Liver Metastasis
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